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J C Porres

Publications and source records attributed to J C Porres.

At least 55 records · Page 3Linked to original sources
PubMed1989

Virus-like particles associated with reverse transcriptase activity in acute sporadic non-A,non-B hepatitis.

Reverse transcriptase activity was tested in 65 patients with non-A,non-B hepatitis, with positive results in 2 acute sporadic cases with favorable outcome. Virus-like particles were observed in ultra-thin sections of successive serum samples from one of the reverse transcriptase activity-positive patients by electron microscopy. These results suggest that some non-A,non-B hepatitis types could be related to a virus-like agent associated with a reverse transcriptase activity.

Adult↗
PubMed1988

Assessment of hepatitis B virus DNA levels in chronic HBsAg carriers with or without hepatitis delta virus superinfection.

In order to document the incidence of hepatitis delta virus (HDV) replication markers and their relationship to HBV replication, 91 HBsAg chronic carriers were studied. Of these, 51 were anti-HD-positive (19 HBeAg-positive and 32 anti-HBe-positive). Liver HDAg was found in 75% of anti-HD-positive patients. Of the 19 patients who had anti-HD and HBeAg, 13 were HBV-DNA-positive. None of the anti-HBe patients were HBV-DNA-positive. No differences with respect to HBV-DNA concentration were observed between anti-HD-positive and -negative patients. Liver HDAg was detected with similar frequency in patients who were HBeAg- and HBV-DNA-positive (63.6%) and in those who were anti-HBe-positive (78.5%), with no statistically significant difference. HBcAg and HDAg were simultaneously detected in 36% of the anti-HD cases. Patients with anti-HD and HBV-DNA had the highest levels of transaminases (SGPT). Our results suggest that in certain patients HDV and HBV replication coexists without mutual inhibition.

Adult↗
PubMed1988

Elevation of 2',5'-oligoadenylate synthetase activity and HLA-I associated beta 2-microglobulin in response to recombinant interferon-gamma administration in chronic HBeAg-positive hepatitis.

We have analyzed the immunomodulatory effect of 5 and 2 MU of recombinant interferon-gamma (rIFN-gamma) administered to 8 carriers of HBsAg with histologically proven chronic active liver disease. After the rIFN-gamma administration, T8 lymphocyte subsets showed a significant decrease (basal vs. 4 weeks, p less than 0.05) and T4/T8 ratios were higher than the basal values in 6/8 patients. Serum levels of the HLA class I-associated beta 2-microglobulin increased significantly in all patients within the first week of treatment, both with the high (p less than 0.01) and the low (p less than 0.05) rIFN-gamma dose. Then, differences between the two doses reached statistical significance (p less than 0.03). Similar results (p less than 0.05) were obtained by measuring the 2',5'-oligoadenylate (2-5A) synthetase activity, co-occurring with the decreases in HBV-DNA polymerase and HBV-DNA, although no differences were found between the two doses. In addition, levels of 2-5A synthetase correlated significantly with those of beta 2-microglobulin (r = 0.743, p less than 0.01). On the other hand, after the rIFN-gamma administration, all the patients had liver membrane antibodies (LMA) in their serum (p less than 0.05); only two patients (who were anti-HD positive) showed LMA at the end of the follow-up. rIFN-gamma has both antiviral and immunomodulatory effects in HBeAg carriers with chronic liver disease.

2',5'-Oligoadenylate Synthetase↗
PubMed1988

Antiviral effect of recombinant gamma interferon in chronic hepatitis B virus infection: a pilot study.

A pilot study has been designed in order to determine the tolerance and effectiveness of recombinant interferon gamma (rIFN-gamma) in chronic hepatitis B virus (HBV) infection. Eight HBsAg, HBeAg, HBV-DNAp and HBV-DNA-positive patients were randomly assigned to one of two groups. In group 1, 0.25 mg of rIFN-gamma/m2 body surface was administered daily for 28 days to 4 patients. In group 2, 0.10 mg of rIFN-gamma was administered to 4 patients under the same conditions. All the patients concluded the treatment and were observed over 11 more months. During treatment, 6 out of 8 patients showed decreased levels of HBV-DNA and HBV-DNAp. In addition, by the 8th month of follow-up, six patients became negative for HBV-DNAp and 2 for HBcAg; all patients remained positive for HBV-DNA. At the end of the study, only 2 patients remained negative for HBV-DNAp, 4 for HBcAg and one became negative for HBV-DNA. No differences in antiviral effect were observed between the two groups. Furthermore, the T4/T8 lymphocytes ratio increased during therapy. In conclusion, rIFN-gamma may play a role in the treatment of chronic HBV infection.

Adult↗
PubMed1988

Different levels of hepatitis B virus replication among hepatitis Be antigen-positive chronic carriers.

Detection of hepatitis B virus DNA polymerase (HBV DNA-pol) activity and of HBV DNA sequences in serum allowed to distinguish the different degrees of HBV replication in chronic HBsAg carriers. The amount of HBV DNA in the serum of 48 HBsAg and HBeAg positive patients in relation with the presence or absence of HBV DNA-pol was determined by dot-blot hybridization. The HBeAg positive cases with HBV DNA-pol activity had significantly higher HBV DNA levels than those which were DNA-pol negative (p less than 0.001). However, no significant differences with respect to liver function tests (transaminase, albumin, gammaglobulin) or to the histological diagnosis were found between both groups. Quantitative detection of serum HBV DNA in HBsAg chronic carriers may be helpful for learning the natural history of HBV infection and monitoring the antiviral therapy.

Carrier State↗
PubMed1988

Different doses of recombinant alpha interferon in the treatment of chronic hepatitis B patients without antibodies against the human immunodeficiency virus.

A total of 24 chronic carriers of HBsAg, HBeAg and hepatitis B virus (HBV)-DNA were included in a controlled trial. The patients were randomly assigned to four groups: Group I (n = 6): control; group II (n = 6): 2.5 MU; group III (n = 6): 5 MU and group IV (n = 6): 10 MU rIFN-alpha/m2 body surface 3 times weekly i.m. during 6 months. At the end of the treatment, all patients under therapy, as well as 4 belonging to the control group, lost HBV-DNA polymerase. HBV-DNA became negative in 3 (50%), 1 (17%), and 2 (33%) patients from groups II, III, and IV, respectively, while all patients from the control group maintained HBV-DNA. At 15 months of follow-up, 6 patients (33%) under therapy (2 from each group) and 1 from the control group remained HBV-DNA-negative. Knodell's index decreased significantly on comparing basal and final liver biopsies among patients in group IV (16.0 +/- 1.9 vs 7.0 +/- 1.9, p less than 0.01), while no changes were observed in the other groups. Five patients (27%) developed anti-IFN antibodies during treatment. In summary, although low doses of rIFN-alpha (2.5-5 MU) had an antiviral effect on HBV replication, only patients treated with 10 MU showed a significant decrease in liver histological activities. In addition, the effectiveness of rIFN-alpha therapy may be negatively influenced by the appearance of anti-IFN antibodies.

Adult↗
PubMed1987

A controlled study of treatment with recombinant interferon alpha in chronic hepatitis B virus infection: induction and maintenance schedules.

To determine the antiviral effect of recombinant-interferon (rIFN)-alpha in hepatitis B virus (HBV) chronic infection, a controlled study was carried out. A total of 20 HBsAg chronic carriers (18 chronic active hepatitis and 2 chronic persistent hepatitis) were included. All of them had remained HBeAg, HBV-DNA and HBV-DNA polymerase (HBV-DNAp) positive at least six months before treatment. The patients were randomly assigned to two groups: control (n = 10), and treatment (n = 10). A dose of 5.5 megaunits of rIFN-alpha/m2 body surface was administered every day for 21 days (induction) and twice a week for six months thereafter (maintenance). No basal differences were observed between the two groups. No case of intolerable toxicity was observed. One treated patient died in a car crash in the second month. At the end of the first week of therapy, 7/10 (70%) of the treated patients became HBV-DNAp negative. However, in the fifth month only 2 patients remained HBV-DNAp negative and also became HBV-DNA and HBeAg negative. In contrast, no changes in viral markers among control cases were observed. In conclusion, rIFN-alpha has an antiviral effect on chronic HBV infection; however, the induction plus maintenance schedule is not useful to obtain a permanent effect.

Chronic Disease↗
PubMed1987

Receptors for polymerized human serum albumin in plasma derived hepatitis B vaccines.

The presence of polymerized human serum albumin receptors (pHSA-R) in two hepatitis B virus (HBV) plasma derived vaccines (HB-Vax, Merck Sharp and Dohme; Hevac-B, Pasteur) was detected by three methods, using pHSA polystyrene coated beads and 125I-anti-HBs (method 1) and polyclonal (method 2) or monoclonal (method 3) peroxidase conjugated anti-HBs. Only a very weak reaction was found for pHSA-R in HB-Vax vaccine when the tests were performed in undiluted vaccine. No reactivity in 1/100 dilution (normally used to test pHSA-R in serum samples) was observed. In contrast, Hevac-B vaccine contained pHSA-R activity in 1/100 dilution as tested by any of the three methods. Furthermore, the level of pHSA-R detected in Hevac-B vaccine is similar to that observed in asymptomatic HBsAg carriers with the same HBsAg concentration. In summary, Hevac-B vaccine contains pHSA-R, whilst HB-Vax shows only weakly reacting pHSA-R, probably insufficient to develop anti-pHSA-R antibodies.

Hepatitis B↗
PubMed1987

Changes of hepatitis B virus (HBV) markers during prolonged recombinant interferon alpha-2A treatment of chronic HBV infection.

Eleven HBsAg chronic carriers were treated with recombinant-interferon (rIFN)-alpha-2A with either 20 X 10(6) (n = 6) or 10 X 10(6) IU/m2 body surface (n = 5), i.m. twice weekly for 6 months. HBV-markers were tested monthly for 15 months. Throughout the follow-up, 6 patients (54%) became HBeAg, HBV-DNAp and HBV-DNA negative (responders). In addition, 8 were HBcAg-negative, 10 anti-HBc-IgM-negative and 2 HBsAg/IgM complexes negative. All patients gave polymerized human serum albumin receptors and HBsAg-positive results. The low rIFN dose seems to be more efficient for clearing HBV-markers than the high dose. Responder patients already showed lower (P less than 0.05) HBsAg concentration and HBsAg/IgM complexes levels in their basal samples as compared to non-responders, and exhibited under rIFN treatment significant decreases (P less than 0.05) in all HBV-markers studied. In conclusion, the most reliable HBV-markers to be assayed in the evaluation of antiviral therapy are HBV-DNA, HBV-DNAp or HBcAg. The testing of pHSA-R, HBsAg/IgM complexes and anti-HBc-IgM does not seem to be very useful.

Adolescent↗
PubMed1987

Identification of different degrees of hepatitis B virus (HBV) replication by serological (HBV-DNAp, HBcAg and HBV-DNA) and histological (HBcAg) methods.

The incidence of HBV-DNA polymerase, HBV-DNA and serum and liver HBcAg in 104 chronic HBsAg carriers was studied. HBV-DNA was the most frequently detected marker, followed by HBcAg and HBV-DNAp. According to their individual or combined presence, four different serological patterns of viral replication were discerned: 53 patients had all these markers, 30 had HBV-DNA but lacked HBV-DNAp (15 with and 15 without HBcAg) and 21 had no such markers detectable. The simultaneous positivity for all of those markers was observed only in HBeAg-positive patients. HBV-DNA alone or along with HBcAg was found in a similar incidence irrespective of the HBe system. Liver HBcAg was found in all but four patients with and in four without HBV-DNA. Viral DNA concentration was significantly (p less than 0.001) higher when HBV-DNAp tested positive. Indeed, HBeAg rather than anti-HBe patients had higher (p less than 0.005) levels of HBV-DNA. In HBeAg-positive patients, the nuclear HBcAg staining was significantly (p less than 0.05) higher when HBV-DNAp tested positive. In DNA polymerase-negative patients, but positive for HBV-DNA, those with or without HBcAg had a similar percentage of core antigen staining. The same distribution was seen in anti-HBe, HBV-DNA-positive patients. However, the mean percentage of hepatocytes displaying cytoplasmic HBcAg did not differ significantly among patients with HBV-DNA, irrespective of the HBe system and the HBV-DNAp status. Such patients had significantly (p less than 0.001) higher ALT levels than those without viral DNA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Prolonged (6 months) treatment of chronic hepatitis B virus infection with recombinant leukocyte A interferon.

Twelve hepatitis B surface antigen (HBsAg), hepatitis B e antigen (HBeAg), hepatitis B virus DNA polymerase (HBV-DNAp) and hepatitis B virus DNA (HBV-DNA) positive patients with chronic active hepatitis (CAH) were treated with doses of either 20 X 10(6) IU/m2 or 10 X 10(6) IU/m2 body surface of recombinant interferon (rIFN)-alpha-2A, I.M., twice a week, during a period of 6 months. No appreciable differences with respect to clinical history, liver function tests and markers of HBV replication between the two groups were apparent at the time of entry into the trial. At the third month of treatment HBV-DNAp became negative in 10 out of 12 patients (83%). After a 15-month follow-up, HBV-DNAp, HBV-DNA and HBeAg were negative in 7 out of 12 patients (38%) (responders). Furthermore, at 24 months, 2 non-responder patients became HBV-DNA and HBV-DNAp negative and one responder lost serum HBsAg. In addition, HBsAg concentration, GPT level and histological Knodell's index decreased significantly in the responder patients, while no changes were observed in non-responders. Five out of six patients who received a low rIFN dose responded to the treatment, and only 2 out of 6 with a higher dose. No unacceptable toxicity was noted in any of the 12 patients. All of them completed the course of treatment. The results suggest that long-term rIFN-alpha-2A therapy has an antiviral effect in CAH due to HBV infection and is well tolerated.

Adult↗
PubMed1987

Liver membrane antibodies in chronic delta hepatitis.

The correlation between the presence of liver membrane antibodies (LMA) and delta superinfection in chronic hepatitis B was studied in 136 chronic hepatitis patients, 20 hepatitis B surface antigen asymptomatic carriers and 50 healthy controls, by testing for the presence of LMA, hepatitis B virus markers and anti-delta (anti-HD). Neither anti-HD nor LMA were detected in controls or in asymptomatic carriers. LMA positivity was statistically higher (p less than 0.001) in anti-HD-positive patients than in those with no anti-HD. Gamma globulin and glutamic pyruvic transaminase values were increased both in anti-HD- and LMA-positive patients with respect to those who were negative. In conclusion, a close association between the positivity to anti-HD and the presence of circulating LMA was found.

Adult↗
PubMed1987

Inhibition of albumin binding to hepatitis B virions by monoclonal antibody to the preS2 domain of the viral envelope.

The binding of polyalbumin to hepatitis B virus (HBV)-associated envelope epitopes has been studied by means of a radioimmunoprecipitation technique. HBV particles were purified from the sera of chronic hepatitis B surface antigen (HBsAg) carriers and labelled through the endogenous HBV-DNA polymerase reaction. Human albumin, polymerized through glutaraldehyde cross-linking, was able to precipitate (100%) labelled HBV at concentrations of 31.2 and 62.5 micrograms/ml, in contrast to monomeric albumin (HSA). This event was further confirmed by immune electron microscopy. The addition of anti-HSA to the mixture HBV plus polyalbumin gave a 100% precipitation in a wide dilution range (15.6-500 micrograms/ml). The binding of polyalbumin (31.2 micrograms/ml) to virions was strongly inhibited (up to 98%) when preincubating with antibody to a glycosylation-dependent preS2 epitope on HBV. The same was accounted (up to 99%) for polyvalent IgG anti-HBs. However, antibodies to the group 'a' and subtype 'd' determinants, as well as anti-preS1 region antibodies, inhibited weakly polyalbumin binding to HBV. The binding site of the inhibitory antibody overlaps probably with neutralizing epitopes. Our findings support the hypothesis that albumin binding plays an important role in the viral life cycle.

Antibodies, Monoclonal↗
PubMed1987

Hepatitis B surface antigen/IgM complexes: relation to receptors for polymerized human serum albumin, hepatitis B virus (HBV) DNA polymerase activity and HBV markers.

The presence and the level of hepatitis B surface antigen (HBsAg)/IgM complexes were determined in 54 chronic HBsAg carriers in relation to receptors for polymerized human serum albumin (pHSA-R) tested by specific radioimmunoassay, and to hepatitis B virus-DNA polymerase (HBV-DNAp). HBsAg/IgM complexes, correlated significantly with the HBsAg concentration but, at a similar HBsAg concentration, significant highest values of HBsAg/IgM complexes were found among HBeAg positive patients. In addition, a significant correlation was found between HBsAg/IgM complex levels, HBeAg titres and HBV-DNAp activity (r = 0.628, p less than 0.001 and r = 0.559, p less than 0.001, respectively). Moreover, a positive linear correlation was found when comparing HBsAg/IgM complexes and pHSA-R levels (r = 0.848, p less than 0.001). Patients who were positive for HBsAg/IgM complexes had a significantly higher glutamate-pyruvate transaminase (GPT) level than those who did not show any complexes. In conclusion, HBsAg/IgM complexes seemed to be indirectly related to HBV replication.

Antigen-Antibody Complex↗
PubMed1986

Receptors for polymerized human serum albumin and other hepatitis B virus markers during acute hepatitis B--predictive value of the outcome of the disease.

Polymerized human serum albumin virus receptors (pHSA-R) HBsAg, HBeAg, antiHBc-IgM, hepatitis B virus (HBV) DNA polymerase activity and HBV-DNA were studied in 47 acute hepatitis B patients, divided into three groups: 26 HBeAg(+) initially, with favorable outcome; 4 HBeAg (+), with chronic outcome; and 17 antiHBe (+), with favorable outcome. In the basal sample only 2 and 8 patients in Group I were HBV-DNAp and HBV-DNA positive, respectively, and became negative during the follow-up. In contrast all patients in Group II remained positive to both HBV-markers. After a one-month follow-up 100% of the patients in Group II were positive for pHSA-R and HBeAg, in contrast to 25% among those with a favorable outcome in Group I (p less than 0.005). Meanwhile, only 6 out of 17 patients in Group III remained positive for pHSA-R. A significant decrease in pHSA-R and HBsAg concentrations was observed in patients from Group I (p less than 0.005 and p less than 0.05, respectively) 15 days after the onset of the disease, while concentrations of both parameters did not vary in Group II. A significant decrease in HBsAg and pHSA-R concentrations was found in patients from Group III after 15 days (p less than 0.05) and one month follow-up (p less than 0.05), respectively. As a result, pHSA-R and HBeAg are the best prognostic indicators in acute hepatitis B. A decrease in HBsAg and pHSA-R concentrations two weeks after the onset may have predictive value.

Acute Disease↗